First record of well-preserved canid coprolites from Eurasia: New insights into the unique ecological niche of Yuanmou Basin.

This study reconstructs the Early Pleistocene paleoenvironment of the Yuanmou Basin through coproecology of the third member of the Yuanmou Formation. We examined 38 exceptionally well-preserved coprolites from a new fossil locality, and attributed the putative defecating agent to the hypercarnivorous diet canid, through geochemical and quantitative analyses. A new ichnogenus and ichnospecies, igen.

Inhibition of miR-186-5p contributes to high glucose-induced injury in AC16 cardiomyocytes.

A growing body of evidence has demonstrated that microRNAs (miRs) have pivotal roles in the pathophysiological development mechanisms of diabetic cardiomyopathy (DCM). Previous studies have demonstrated that miR-186-5p was significantly decreased in DCM. In addition, it has recently been reported that an imbalance of miR-186 is associated with a variety of physiological and pathological processes.

New mechanism of lipotoxicity in diabetic cardiomyopathy: Deficiency of Endogenous HS Production and ER stress.

Objective: To investigate the roles and mechanisms of endogenous hydrogen sulfide (HS) and endoplasmic reticulum (ER) stress in the development of diabetic cardiomyopathy (DCM).

Methods: Blood of DCM patients included in the study were collected. The model of DCM rats was established using streptozotocin (STZ) injection.

Naringin protects cardiomyocytes against hyperglycemia-induced injuries in vitro and in vivo.

We previously reported that naringin (NRG) protects cardiomyocytes against high glucose (HG)-induced injuries by inhibiting the MAPK pathway. The aim of this study was to test the hypothesis that NRG prevents cardiomyocytes from hyperglycemia-induced insult through the inhibition of the nuclear factor kappa B (NF-κB) pathway and the upregulation of ATP-sensitive K(+) (KATP) channels. Our results showed that exposure of cardiomyocytes to HG for 24h markedly induced injuries, as evidenced by a decrease in cell viability and oxidative stress, and increases in apoptotic cells as well as the dissipation of mitochondrial membrane potential (MMP).

Inhibition of the leptin-induced activation of the p38 MAPK pathway contributes to the protective effects of naringin against high glucose-induced injury in H9c2 cardiac cells.

Leptin, a product of the obese gene, has been reported to contribute to the development of cardiomyocyte hypertrophy in patients with diabetes and to activate the p38 mitogen-activated protein kinase (MAPK) pathway in cardiomyocytes. In this study, we demonstrate that naringin, a citrus flavonone, protects cardiomyoblasts (H9c2 cells) against high glucose (HG)-induced apoptosis by modulating the activation of the p38 MAPK pathway. We investigated the hypothesis that naringin prevents HG-induced injury by inhibiting the leptin-induced activation of the p38 MAPK pathway in H9c2 cells.

Naringin inhibits ROS-activated MAPK pathway in high glucose-induced injuries in H9c2 cardiac cells.

Naringin, an active flavonoid isolated from citrus fruit extracts, exhibits biological and pharmacological properties, such as antioxidant activity and antidiabetic effect. Mitogen-activated protein kinase (MAPK) signalling pathway has been shown to participate in hyperglycaemia-induced injury. The present study tested the hypothesis that naringin protects against high glucose (HG)-induced injuries by inhibiting MAPK pathway in H9c2 cardiac cells.

Angiographic and interventional management for a esophagopericardial fistula.

We reported a case of a 78-year-old patient with esophagopericardial fistula who was referred for angiographic and interventional management. Emergent implantation of the esophageal stent could not lengthen or even save the patient's life. One week later, the patient died of multiple organ failure, which was probably from formation of granulation tissue and stent migration.

Naringin inhibits high glucose-induced cardiomyocyte apoptosis by attenuating mitochondrial dysfunction and modulating the activation of the p38 signaling pathway.

Recently, naringin (NAR; 4',5,7-trihydroxyflavanone-7-rhamnoglucoside) has been shown to have cardioprotective properties. However, the specific mechanisms underlying its cardioprotective effects remain unclear. In this study, we aimed to investigate the cardioprotective effects of NAR and the possible underlying molecular mechanisms in cardiomyocytes using high glucose (HG) to induce apoptosis in H9c2 cells.

Protective effect of curcumin against cardiac dysfunction in sepsis rats.

Context: The heart is one of the target organs susceptible to attack by sepsis, and protection of the cardiac function in sepsis or alleviation dysfunction caused by sepsis appears a serious and urgent problem.

Objective: This study was designed to explore the effect of curcumin on myocardial injury induced by sepsis and to explore the therapeutic effect of curcumin in managing sepsis induced cardiac dysfunction.

Methods: Cecal ligation and puncture surgery were used to establish the sepsis model.

Increased expression of heat shock protein 90 under chemical hypoxic conditions protects cardiomyocytes against injury induced by serum and glucose deprivation.

Heat shock proteins (HSPs) are critical for adaptation to hypoxia and/or ischemia. Previously, we demonstrated that cobalt chloride (CoCl2), a well-known hypoxia mimetic agent, is an inducer of HSP90. In the present study, we tested the hypothesis that CoCl₂-induced upregulation of HSP90 is able to provide cardioprotection in serum and glucose-deprived H9c2 cardiomyocytes (H9c2 cells).

[Expression of Toll-like receptor 4 and tumor necrosis factor-α on peripheral-blood mononuclear cells and their correlation with myocardial perfusion in patients with diabetic cardiomyopathy].

Objective: To explore the expression of Toll-like receptor 4 (TLR4) and tumor necrosis factor-α (TNF-α) on peripheral-blood mononuclear cells (PBMCs) and their correlation with myocardial perfusion in patients with diabetic cardiomyopathy (DCM).

Methods: The expression of TLR4 and TNF-α mRNA on PBMCs were examined by SYBR Green I real-time quantitative reverse transcription polymerase chain reaction (RT-PCR), the levels of TLR4 and TNF-α were examined by flow cytometric analysis and enzyme-linked immuno sorbent assay (ELISA) on DCM group (n = 20), Type 2 diabetic group (n = 22) and control group (n = 20). Myocardial perfusion was visualized by single-photon emission computed tomography (SPECT).